A variety of abnormalities of hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal (HPA) function have been described in patients with anorexia nervosa (AN). Two abnormalities which may reflect hypothalamic disturbance are age-inappropriate, immature circadian patterns of luteinizing hormone secretion and increased levels of adrenocortical activity. However, the nature of the association between these endocrine abnormalities and the syndrome of AN is obscure. The type and the severity of these endocrine disturbances may be specific hallmarks of the syndrome of AN. Or these disturbances may be non-specifically associated with certain individual features of the syndrome, such as weight loss. We propose to examine the association between the syndrome of AN and these HPG and H abnormalities by testing two hypothesis: (1) that the nature of the HPG disturbance in AN is unique to the AN syndrome, and (2) that the degree of HPA disturbance in AN is greater than would be predicted on the basis of the clinical features of the syndrome considered individually. Our strategy for testing these hypotheses is to conduct clinical studies of HPG and HPA function in women who do not have the full syndrome of AN but who exhibit one or several features of the syndrome. For example, we propose to study women of low body weight who do not show distorted body image or obsessive preoccupation with food and weight. If such women are found to have the same types and degrees of HPG and HPA dysfunction as women with AN, we can conclude these endocrine disturbances are not unique to the AN syndrome but are related to the non-specific feature, namely weight loss. The clinical features we will focus on are decreased body weight, disturbed eating behavior, distortion of body image, increased physical activity, and acute psychological stress. The methods we will use include psychological and behavioral ratings, determination of the circadian pattern of luteinizing hormone secretion, and measurement of the cortisol production rate and of the response of plasma cortisol to suppression by dexamethasone.